In a previous patent application (patent application Ser. No.: 9500519-5, Filing Date: May 5, 1995), the use of des-Aspartate-angiotensin I as an anti-cardiac hypertrophic agent was described. In the embodiments shown in the previous patent application, des-Aspartate-angiotensin I, administered either intravenously or orally, significantly and dose-dependently attenuated the cardiac hypertrophy in experimentally-induced cardiac hypertrophic rats. Therefore, the invention in the previous patent was directed to the use of des-Aspartate-angiotensin I as an anti-cardiac hypertrophic agent.
Des-Aspartate-angiotensin I has been shown to act on a specific indomethacin-sensitive subtype of angiotensin receptor (Sim and Chai, Br. J. Pharmacol., 117:1504-1506 (1996)), and to antagonize the pressor (Sim and Radhakrishnan, Eur. J. Pharmacol., 257:R1-R3 (1994)), and hypertrophic (Min and Sim, Asia Pacific J. Pharmacol. 12:S23 (1997)) actions of angiotensin II. As angiotensin II has either a direct or promotive role in the formation of neointima in balloon catheter-injured blood vessels (Osterrieder et al, Hypertension, 18:II-60-II-64 (1991); Daemen et al, Circ. Res., 68:450-456 (1991)), and chronic development of arteriosclerosis in animals and man (Pitt, Eur Heart J. 16 (Suppl K):49-54 (1995); Timmis and Pitt, Br. Heart J. 72 (Suppl):57-60 (1994)), it is possible that des-Aspartate-angiotensin I could, through its anti-angiotensin II actions, prevent or attenuate the formation of neointima in balloon catheter-injured blood vessels and the chronic development of arteriosclerosis in hypertensive animals and humans.